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Caveolin-1 ameliorates acetaminophen-aggravated inflammatory damage and lipid deposition in non-alcoholic fatty liver disease via the ROS/TXNIP/NLRP3 pathway
Int Immunopharmacol. 2023 Jan;114:109558. doi: 10.1016/j.intimp.2022.109558. Epub 2022 Dec 21.ABSTRACTThe overuse of acetaminophen (APAP) may cause more severe hepatotoxicity in patients with non-alcoholic fatty liver disease (NAFLD). Caveolin-1 (CAV1), is an essential regulator of metabolic function, which can alleviate liver damage by scavenging reactive oxygen species (ROS). Evidence suggests that the NOD-like receptor family pyrin domain-containing 3 (NLRP3) -mediated pyroptosis is involved in the development of NAFLD. Moreover, thioredoxin-interactive protein (TXNIP) activation is a key event linking ROS to NLRP3 infl...
Source: International Immunopharmacology - January 26, 2023 Category: Allergy & Immunology Authors: Xiangfu Jiang Yu Li Dongdong Fu Tingyu You Shuai Wu Jiao Xin Jiagen Wen Yan Huang Chengmu Hu Source Type: research

Caveolin-1 alleviates acetaminophen-induced vascular oxidative stress and inflammation in non-alcoholic fatty liver disease
In conclusion, our findings confirmed that CAV1 exerts a protective effect against vascular injury by inhibiting oxidative stress and inflammation through the PKC/MAPK pathway. Therefore, restoration of CAV1 may have clinical benefits in reducing APAP-induced vascular damage in NAFLD patients.PMID:36596386 | DOI:10.1016/j.freeradbiomed.2022.12.095
Source: Free Radical Biology and Medicine - January 3, 2023 Category: Biology Authors: Dongdong Fu Shuai Wu Xiangfu Jiang Tingyu You Yu Li Jiao Xin Xiaowen Feng Jiagen Wen Yan Huang Chengmu Hu Source Type: research

Caveolin-1 Alleviates Acetaminophen-Induced Fat Accumulation in Non-Alcoholic Fatty Liver Disease by Enhancing Hepatic Antioxidant Ability via Activating AMPK Pathway
In this study, seven-week-old C57BL/6 male mice (18–20 g) were raised under similar conditions for in vivo experiment. In vitro, L02 cells were treated with A/O (alcohol and oleic acid mixture) for 48 h, and APAP was added at 24 h for further incubation. The results showed that the protein expression of the AMPK/Nrf2 pathway was enhanced after CAV1 upregulation. The effects of CAV1 on fat accumulation, ROS, and the AMPK/Nrf2 anti-oxidative pathway were reduced after the application of CAV1-siRNA. Finally, treatment with compound C (an AMPK inhibitor) prevented CAV1 plasmid-mediated alleviation of oxidative stress and ...
Source: Frontiers in Pharmacology - July 7, 2021 Category: Drugs & Pharmacology Source Type: research